Distribution and release of peptide YY in dog measured by specific radioimmunoassay

Taylor, Ian L.

doi:10.1016/0016-5085(85)90144-1

Cited by 169 publications

(65 citation statements)

References 13 publications

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“…NPY-like immunoreactivity (NPY-LI) is present in nerve fibres and occasional ganglion cells of both myenteric and submucosal plexi in the colon of most mammalian species so far studied, including pig and man (Furness et al, 1983;Ferri et al, 1984). PYY-LI is localized to mucosal endocrine cells in mammalian colon (Lundberg et al, 1982) and is released into the circulation following the ingestion of a meal (Taylor, 1985;Greeley et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

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Localization and characterization of neuropeptide Y binding sites in porcine and human colon

Walsh

Wharton²,

Blake

et al. 1993

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

“…PYY-LI is released into the systemic circulation in mammals following feeding (Adrian et al, 1985;Taylor, 1985), and may therefore act as a circulating hormone. In addition, local release of NPY and PYY may serve paracrine, autocrine or neurotransmitter functions.…”

Section: Introductionmentioning

confidence: 99%

Localization and characterization of neuropeptide Y binding sites in porcine and human colon

Walsh

Wharton²,

Blake

et al. 1993

British J Pharmacology

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“…PYY is synthesized in the gastrointestinal tract, as well as in the central and peripheral nervous systems. Endocrine cells of the ileum, colon, and rectum provide a major source of PYY (2,47). PYY has also been detected in gastric mucosa, pancreatic islets, myenteric and serosal ganglia, sympathetic neurons, adrenal gland, spinal cord, and brain, including the hypothalamus, pituitary, pons, medulla oblongata, and the brain stem (7-9, 15, 16, 22, 30, 32, 37).…”

mentioning

confidence: 99%

“…Food intake releases PYY into the circulation (2,47). Systemic administration of PYY inhibits food intake, gastric emptying, intestinal fluid and electrolyte secretion, gallbladder contraction, and exocrine pancreatic secretion (5,36).…”

mentioning

confidence: 99%

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Chelikani

Haver²,

Reidelberger³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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We compared the effects of the two molecular forms of the brain-gut peptide YY (PYY), PYY(1-36) and PYY(3-36), on gastric emptying. Unanesthetized rats received 20-min intravenous infusions of rat PYY(1-36) (0, 1.7, 5, 17, 50, 100, 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and rat PYY(3-36) (0, 0.5, 1.7, 5, 17, 50, 100, 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ), either alone or combined, and gastric emptying of saline was measured during the last 10 min of infusion. For comparison, human PYY(3-36) was administered at 0, 17, and 50 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 . Gastric emptying was decreased by 11, 24, 26 and 38% in response to 17, 50, 100, and 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of rat PYY(1-36); by 10, 26, 41, 53, and 57% in response to 5, 17, 50, 100, and 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of rat PYY(3-36); and by 35 and 53% in response to 17 and 50 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of human PYY(3-36), respectively. Estimated ED50s were 470 and 37 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 for rat PYY(1-36) and PYY(3-36), respectively. In general, within an experiment, coadministration of PYY(1-36) and PYY(3-36) inhibited gastric emptying by an amount that was comparable to that produced when either peptide was given alone. We conclude that 1) intravenous infusion of PYY(1-36) and PYY(3-36) each produces a dose-dependent inhibition of gastric emptying in rats, 2) PYY(3-36) is an order of magnitude more potent than PYY(1-36) in inhibiting gastric emptying, 3) human PYY(3-36) and rat PYY(3-36) inhibit gastric emptying similarly, and 4) PYY(1-36) and PYY(3-36) do not appear to interact in an additive or synergistic manner to inhibit gastric emptying. intravenous infusion; dose response; interaction PEPTIDE YY (PYY), neuropeptide Y (NPY), and pancreatic polypeptide (PP) comprise the "PP-fold" family of structurally related brain-gut peptides. PYY is synthesized in the gastrointestinal tract, as well as in the central and peripheral nervous systems. Endocrine cells of the ileum, colon, and rectum provide a major source of PYY (2, 47). PYY has also been detected in gastric mucosa, pancreatic islets, myenteric and serosal ganglia, sympathetic neurons, adrenal gland, spinal cord, and brain, including the hypothalamus, pituitary, pons, medulla oblongata, and the brain stem (7-9, 15, 16, 22, 30, 32, 37).Food intake releases PYY into the circulation (2, 47). Systemic administration of PYY inhibits food intake, gastric emptying, intestinal fluid and electrolyte secretion, gallbladder contraction, and exocrine pancreatic secretion (5, 36). Whether PYY acts physiologically by endocrine, neurocrine, and/or paracrine mechanisms to produce these effects remains to be determined. If PYY acts as a blood-borne hormonal signal to produce an effect, then it is important to determine whether the effect is produced by intravenous doses of PYY that reproduce meal-induced increases in plasma PYY.The two major molecular forms of PYY found in the gut and circulation are PYY(1-36) and PYY(3-36) (19 -21). In humans, plasma concentrations of PYY were reported to be 11 pM in the fasted state with PYY(3-36) contributing 37% ...

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“…Plasma levels of PYY have previously been shown to increase within an hour after food intake in humans (from approximately 8 to 45 pmol/1) and in the dog (from approximately 200 to 400 pmol/1) [34,35]. In the dog, PYY inhibits stimulated insulin secretion at concentrations within this range [10,11].…”

Section: Ag Nieuwenhuizen Et Al: Peptide Yy and Insulin Secretionmentioning

confidence: 94%

Mechanisms underlying the insulinostatic effect of peptide YY in mouse pancreatic islets

Nieuwenhuizen¹,

Karlsson²,

Fridolf³

et al. 1994

Diabetologia

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Summary Peptide YY is an insulinostatic peptide which is released into the circulation from the intestinal mucosa upon food intake. Peptide YY is also co-stored with glucagon in the secretory granules of the pancreatic alpha cells. We examined the mechanisms underlying the insulinostatic effect of peptide YY in isolated mouse pancreatic islets. We found that peptide YY (0.1 nmol/1-1 ~tmol/1) inhibited glucose (11.1 mmol/1)-stimulated insulin secretion from incubated isolated islets, with a maximal inhibition of approximately 70 % observed at a dose of 1 nmol/ 1 (p < 0.001). Also in perifused islets the peptide (1 nmol/1) inhibited insulin secretion in response to 11.1 mmol/1 glucose (p < 0.001). Furthermore, peptide YY inhibited glucose-stimulated cyclic AMP formation (by 67 %, p < 0.05), and insulin secretion stimulated by dibutyryl cyclic AMP (p < 0.01). In contrast, the peptide was without effect both on the cytoplasmic Ca 2 + concentration in dispersed mouse isletcell suspensions as measured by the FURA 2-AM technique, and on insulin release in isolated islets, when stimulated by the protein kinase C-activator 12-O-tetradecanoyl phorbol 13-acetate. Finally, in pre-labelled perifused islets, peptide YY caused a small and transient increase in the 86Rb+ efflux (p < 0.001), but only in the absence of extracellular Ca 2 +. We conclude that peptide YY inhibits glucosestimulated insulin secretion from isolated mouse islets by inhibiting two different steps in the cyclic AMP cascade, that is, both the accumulation and the action of the cyclic nucleotide. In contrast, the data suggest that protein kinase C, K + channels, the cytoplasmic Ca 2 + concentration or other processes directly regulating the exocytosis are not involved in the signal transduction underlying peptide YY-induced inhibition of insulin secretion. [Diabetologia (1994) [4,5]. Recently, PYY has been localized to the alpha cells in both the mouse and the rat pancreas [6,7], where it is co-stored with glucagon in the secretory granules [8]. The peptide has previously been demonstrated to inhibit stimulated insulin secretion under in vivo conditions in the rat [9], dog [10,11] and mouse [8], and in vitro in the perfused isolated rat pancreas and in isolatedrat islets [12]. This suggests that PYY participates in the regulation of insulin secretion.In the present study, we have examined possible mechanisms underlying the inhibitory effect of PYY

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Distribution and release of peptide YY in dog measured by specific radioimmunoassay

Cited by 169 publications

References 13 publications

Localization and characterization of neuropeptide Y binding sites in porcine and human colon

Localization and characterization of neuropeptide Y binding sites in porcine and human colon

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Mechanisms underlying the insulinostatic effect of peptide YY in mouse pancreatic islets

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